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Article Abstract
In response to Zn deficiency, plants are thought to adjust Zn homeostasis through the coordinated expression of Zn transporters. Zn transporters are identified in the ZIP, HMA and CDF families of cation transporters, although only few are characterized. We determined gene expression over time, root-specific location of expression and phenotypes of single and double loss-of-function mutants of several Arabidopsis thaliana transporters, known to be induced by Zn deficiency. Transcription of Zn transporter genes is induced in the first 6 h of exposure to Zn deficiency. ZIP1 is predominantly expressed in the endodermis and stele, ZIP3 and ZIP5 in the epidermis and cortex, IRT3 from epidermis to stele and HMA2 in xylem parenchyma. ZIP3 and ZIP5 act redundantly, with the double-mutant zip3zip5 showing high sensitivity to Zn deficiency with low biomass production, expression of other transporter genes, low Zn uptake and increased metal translocation. The root expression map and timing indicate that Zn transporters act complementary in a concerted action to control Zn homeostasis. The lack of strong Zn-deficient phenotypes in single mutants suggests a high level of functional redundancy, best illustrated for ZIP3 and ZIP5.
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| http://dx.doi.org/10.1111/tpj.17251 | DOI Listing |
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Article Synopsis
- A recent study explored how zinc (Zn) and amino acid transporters enhance Zn absorption in broiler chickens using a specific form of zinc called Zn proteinate with moderate chelation strength.
- The research involved three experiments to evaluate how Zn-Prot M and traditional Zn sulfate (ZnS) influenced Zn absorption and transporter expression in cells from the duodenum of broiler embryos.
- Results indicated that optimal conditions for Zn absorption were identified, with Zn-Prot M leading to significantly greater absorption compared to Zn sulfate under certain concentrations and incubation times.